Posts Tagged Vagal nerve stimulation

[Abstract + References] Antidepressant effect of vagal nerve stimulation in epilepsy patients: a systematic review

Abstract

Background

Vagal nerve stimulation (VNS) is an effective palliative therapy in drug-resistant epileptic patients and is also approved as a therapy for treatment-resistant depression. Depression is a frequent comorbidity in epilepsy and it affects the quality of life of patients more than the seizure frequency itself. The aim of this systematic review is to analyze the available literature about the VNS effect on depressive symptoms in epileptic patients.

Material and methods

A comprehensive search of PubMed, Medline, Scopus, and Google Scholar was performed, and results were included up to January 2020. All studies concerning depressive symptom assessment in epileptic patients treated with VNS were included.

Results

Nine studies were included because they fulfilled inclusion criteria. Six out of nine papers reported a positive effect of VNS on depressive symptoms. Eight out of nine studies did not find any correlation between seizure reduction and depressive symptom amelioration, as induced by VNS. Clinical scales for depression, drug regimens, and age of patients were broadly different among the examined studies.

Conclusions

Reviewed studies strongly suggest that VNS ameliorates depressive symptoms in drug-resistant epileptic patients and that the VNS effect on depression is uncorrelated to seizure response. However, more rigorous studies addressing this issue are encouraged.

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Source: https://link.springer.com/article/10.1007/s10072-020-04479-2

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[WEB SITE] Vagal Nerve Stimulation Improves Arm Function After Stroke

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HOUSTON, Texas — An implanted device that stimulates the vagus nerve has shown promising improvement of arm function in stroke patients in a second small clinical study.

While the primary endpoint — change in functional score after 6 weeks of therapy — was not significantly different between treatment groups, the improvement did appear to become significant after a further 60 days of treatment, as did responder rates.

Lead investigator, Jesse Dawson, MD, University of Glasgow, United Kingdom, reported that the group receiving active stimulation with the device showed a 9-point improvement in upper-limb Fugl-Meyer (UEFM) score at this time point.

Dr Jesse Dawson

“All in all, we feel this is quite promising,” Dr Dawson said. “A 9-point change in this scale is highly likely to be clinically significant.”

This magnitude of change would mean different things for different patients, depending on where they start, he said. “If they start at 20 — which is not much function at all — they might regain some grasp ability so they might be able to carry a plate, for example. If they were in the 30s to start with, they would probably already have the grasp function but they would be able to get back to do more specific tasks.”

The results were presented here at the International Stroke Conference (ISC) 2017.

“Spectacular” Results

Commenting on the study, American Heart Association/American Stroke Association spokesperson, Philip Gorelick, MD, MPH, medical director, Hauenstein Neuroscience Center, Grand Rapids, Michigan, described the results as “pretty spectacular.”

Dr Philip Gorelick

“It is always difficult to know what you are getting with these scales, but when you see jumps like this I think it’s safe to conclude that there is clinical significance. There is probably something real going on,” Dr Gorelick said.

“You must remember that these are chronic patients with moderate to severe arm weakness at 18 months down the line from their stroke,” he added. “We think these patients are finished — they are not going to be doing much with that arm. Obviously this study is exploratory, but this raises a lot of hope.”

A larger trial in 120 patients is now planned.

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[Abstract] Non electrical and non pharmacological ways of vagus nerve stimulation: Overview, pathways and clinical implications

Vagal nerve stimulation is gaining recognition as an important therapeutic approach especially for non-communicable diseases such as cardiovascular disease (CVD), Depression, Fibromyalgia, Arthritis, Type 2 Diabetes, Alzheimer, and certain types of cancer. In turn, decreased vagal tone its implicated in the prognosis of a wide range of diseases. Afferent vagal stimulation seems to have the key to reset certain pathophysiological states of the body leading to health improvement by reshaping neural networks.

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via Non electrical and non pharmacological ways of vagus nerve stimulation: Overview, pathways and clinical implications – Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation

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[Abstract + References] Improving Stroke Rehabilitation with Vagus Nerve Stimulation

Abstract

Stroke is a leading cause of neurological damage, with an estimated 795,000 cases reported in the United States each year. A large percentage of patients who suffer a stroke exhibit long-term impairments in motor function. Poststroke rehabilitation in part aims to promote adaptive changes in neural circuits to support recovery of function, but insufficient or maladaptive plasticity often limits benefits. Adjunctive strategies that support plasticity in conjunction with rehabilitation represent a potential means to improve recovery after stroke. Vagus nerve stimulation (VNS) has emerged as one such targeted plasticity strategy, providing phasic activation of neuromodulatory nuclei associated with plasticity. Repeatedly pairing brief bursts of VNS with motor training drives robust, specific plasticity in neural circuits. A number of studies in animal models of stroke and neurological injury demonstrate that VNS paired with rehabilitative training improves recovery of motor function. Moreover, emerging evidence from clinical trials indicates that VNS delivered during rehabilitation promotes functional recovery in stroke patients. Here, we provide a discussion of the existing literature of VNS-based targeted plasticity therapies in the context of stroke and outline challenges for clinical implementation.

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via Improving Stroke Rehabilitation with Vagus Nerve Stimulation | SpringerLink

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[Abstract] The interaction of pulse width and current intensity on the extent of cortical plasticity evoked by vagus nerve stimulation.

Abstract

Background

Repeatedly pairing a tone with a brief burst of vagus nerve stimulation (VNS) results in a reorganization of primary auditory cortex (A1). The plasticity-enhancing and memory-enhancing effects of VNS follow an inverted-U response to stimulation intensity, in which moderate intensity currents yield greater effects than low or high intensity currents. It is not known how other stimulation parameters effect the plasticity-enhancing effects of VNS.

Objective

We sought to investigate the effect of pulse-width and intensity on VNS efficacy. Here, we used the extent of plasticity induced by VNS-tone pairing to assess VNS efficacy.

Methods

Rats were exposed to a 9 kHz tone paired to VNS with varying current intensities and pulse widths. Cortical plasticity was measured as changes in the percent of area of primary auditory cortex responding to a range of sounds in VNS-treated rats relative to naïve rats.

Results

We find that a combination of low current intensity (200 μA) and short pulse duration (100 μs) is insufficient to drive cortical plasticity. Increasing the pulse duration to 500 μs results in a reorganization of receptive fields in A1 auditory cortex. The extent of plasticity engaged under these conditions is less than that driven by conditions previously reported to drive robust plasticity (800 μA with 100 μs wide pulses).

Conclusion

These results suggest that the plasticity-enhancing and memory-enhancing effects of VNS follow an inverted-U response of stimulation current that is influenced by pulse width. Furthermore, shorter pulse widths may offer a clinical advantage when determining optimal stimulation current. These findings may facilitate determination of optimal VNS parameters for clinical application.

via The interaction of pulse width and current intensity on the extent of cortical plasticity evoked by vagus nerve stimulation – Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation

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[WEB SITE] Epilepsy and Seizures: Practice Essentials, Background, Pathophysiology – Medscape

Epileptic seizures are only one manifestation of neurologic or metabolic diseases. Epileptic seizures have many causes, including a genetic predisposition for certain types of seizures, head trauma, stroke, brain tumors, alcohol or drug withdrawal, repeated episodes of metabolic insults, such as hypoglycemia, and other conditions.

Epilepsy and Seizures

  • Author: David Y Ko, MD; Chief Editor: Selim R Benbadis, MD  more…
Updated: Nov 19, 2015

Practice Essentials

Epilepsy is defined as a brain disorder characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition.[1]

Signs and symptoms

The clinical signs and symptoms of seizures depend on the location of the epileptic discharges in the cerebral cortex and the extent and pattern of the propagation of the epileptic discharge in the brain. A key feature of epileptic seizures is their stereotypic nature.

Questions that help clarify the type of seizure include the following:

  • Was any warning noted before the spell? If so, what kind of warning occurred?
  • What did the patient do during the spell?
  • Was the patient able to relate to the environment during the spell and/or does the patient have recollection of the spell?
  • How did the patient feel after the spell? How long did it take for the patient to get back to baseline condition?
  • How long did the spell last?
  • How frequent do the spells occur?
  • Are any precipitants associated with the spells?
  • Has the patient shown any response to therapy for the spells?

See Clinical Presentation for more detail.

Diagnosis

The diagnosis of epileptic seizures is made by analyzing the patient’s detailed clinical history and by performing ancillary tests for confirmation. Physical examination helps in the diagnosis of specific epileptic syndromes that cause abnormal findings, such as dermatologic abnormalities (eg, patients with intractable generalized tonic-clonic seizures for years are likely to have injuries requiring stitches).

Testing

Potentially useful laboratory tests for patients with suspected epileptic seizures include the following:

  • Prolactin levels obtained shortly after a seizure to assess the etiology (epileptic vs nonepileptic) of a spell; levels are typically elevated 3- or 4-fold and more likely to occur with generalized tonic-clonic seizures than with other seizure types; however, the considerable variability of prolactin levels has precluded their routine clinical use
  • Serum levels of anticonvulsant agents to determine baseline levels, potential toxicity, lack of efficacy, treatment noncompliance, and/or autoinduction or pharmacokinetic change
  • CSF examination in patients with obtundation or in patients in whom meningitis or encephalitis is suspected

Imaging studies

The following 2 imaging studies must be performed after a seizure:

  • Neuroimaging evaluation (eg, MRI, CT scanning)
  • EEG

The clinical diagnosis can be confirmed by abnormalities on the interictal EEG, but these abnormalities could be present in otherwise healthy individuals, and their absence does not exclude the diagnosis of epilepsy.

Video-EEG monitoring is the standard test for classifying the type of seizure or syndrome or to diagnose pseudoseizures (ie, to establish a definitive diagnosis of spells with impairment of consciousness). This technique is also used to characterize the type of seizure and epileptic syndrome to optimize pharmacologic treatment and for presurgical workup.

See Workup for more detail.

Management

Pharmacotherapy

The goal of treatment is to achieve a seizure-free status without adverse effects. Monotherapy is important, because it decreases the likelihood of adverse effects and avoids drug interactions.

Standard of care for a single, unprovoked seizure is avoidance of typical precipitants (eg, alcohol, sleep deprivation). No anticonvulsants are recommended unless the patient has risk factors for recurrence.

Special situations that require treatment include the following:

  • Recurrent unprovoked seizures: The mainstay of therapy is an anticonvulsant; if a patient has had more than 1 seizure, administration of an anticonvulsant is recommended
  • Having an abnormal sleep-deprived EEG that includes epileptiform abnormalities and focal slowing, diffuse background slowing, and intermittent diffuse intermixed slowing

Selection of an anticonvulsant medication depends on an accurate diagnosis of the epileptic syndrome. Although some anticonvulsants (eg, lamotrigine, topiramate, valproic acid, zonisamide) have multiple mechanisms of action, and some (eg, phenytoin, carbamazepine, ethosuximide) have only one known mechanism of action, anticonvulsant agents can be divided into large groups based on their mechanisms, as follows:

  • Blockers of repetitive activation of the sodium channel: Phenytoin, carbamazepine, oxcarbazepine, lamotrigine, topiramate
  • Enhancer of slow inactivation of the sodium channel: Lacosamide, rufinamide
  • Gamma aminobutyric acid (GABA)–A receptor enhancers: Phenobarbital, benzodiazepines, clobazam
  • NMDA receptor blockers: Felbamate
  • AMPA receptor blockers: Perampanel, topiramate
  • T-calcium channel blockers: Ethosuximide, valproate
  • N- and L-calcium channel blockers: Lamotrigine, topiramate, zonisamide, valproate
  • H-current modulators: Gabapentin, lamotrigine
  • Blockers of unique binding sites: Gabapentin, levetiracetam
  • Carbonic anhydrase inhibitors: Topiramate, zonisamide
  • Neuronal potassium channel (KCNQ [Kv7]) opener: Ezogabine

Nonpharmacologic therapy

The following are 2 nonpharmacologic methods in managing patients with seizures:

  • A ketogenic diet
  • Vagal nerve stimulation

Surgical options

The 2 major kinds of brain surgery for epilepsy are palliative and potentially curative. The use of a vagal nerve stimulator (VNS) for palliative therapy in patients with intractable atonic seizures has reduced the need for anterior callosotomy. Lobectomy and lesionectomy are among several possible curative surgeries.

See Treatment and Medication for more detail.

Source: Epilepsy and Seizures: Practice Essentials, Background, Pathophysiology

 

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